Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/13839
Title: Metabotropic glutamate receptor 1-alpha: Modulation of soman-induced status epilepticus
Authors: LEONG AI LIN
Keywords: Soman; status epilepticus; metabotropic glutamate receptor; LY367385; glutamate; GABA.
Issue Date: 12-Mar-2004
Source: LEONG AI LIN (2004-03-12). Metabotropic glutamate receptor 1-alpha: Modulation of soman-induced status epilepticus. ScholarBank@NUS Repository.
Abstract: Soman (pinacolyl methylphosphonofluoridate), a potent irreversible acetylcholinesterase inhibitor, induces status epilepticus (SISE) in rats during severe intoxication. Subsequent neurodegeneration in limbic structures is a result of hyperexcitability of the epileptic brain and was thought to be mediated by activation of glutamate receptors. Immunohistology staining of brain sections obtained from rats subjected to convulsive dose (176A?g/ kg, s.c. ) of soman showed a 3-fold up- regulation of metabotropic glutamate receptor 1-alpha at 8 hours post-SISE. Post-seizure treatment with mGluR1-alpha specific antagonist, LY367385 (400 nmole, icv.), and diazepam (4 mg/ kg, i.m.) terminated seizure activity and conferred neuroprotection to half of the animals tested (n = 6). Reverse microdialysis of LY367385 into the piriform cortex enhanced GABA release and inhibited glutamate output. For glutamate, both that basal output of non-intoxicated and enhanced output of soman-intoxicated rats were inhibited. The data indicate that selective antagonism of mGluR1 provides neuroprotection in part through modulation of neurotransmitters release.
URI: http://scholarbank.nus.edu.sg/handle/10635/13839
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